Localized and dynamic repolarization alternans in Ajmaline accentuated Brugada syndrome

Acquired long QT syndrome: Risperidone-facilitated triggered activity and Torsades de Pointes during complete AV block. I

“…The surface ECG tracings so far presented support the contention that the U wave is not a separate entity, but a component of the T wave, whose 2nd part, ascending (or descending) limb, is interrupted [3]. Alterations in repolarization currents secondary to genetic defects (cLQTS) [20], or exposed after drug challenge [21,22] may be translated to the surface ECG, making its content less empirical and more cell-biology based [23].…”

Acquired long QT syndrome: Unequal regression of Amiodarone-induced repolarization lengthening

“…In Na + channel variant syndromes (LQTS3, manifest or drug-accentuated Brugada Syndrome, Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia? ), the "electrical participation" of the RV (or of its outflow tract), as observed in surface transmural ECGs, is remarkable [13,14]. The factors so far presented, specially if acting in concert, could lead to a decrease of I Ks expression in RV, outweighing, (if present in the human heart), the larger content in I K s [2], and prolonging APD and repolarization time in that area.…”

Adrenergic-mediated exposure of hyperkalemia in the electrocardiogram

“….) [11]. Regarding findings in molecular biology, it has been reported that the h-AR modulation of I Ks requires targeting of cAMP dependent PKA and protein phosphatase to I Ks channel subunits (hKCNQ1, hKCNE1, the genes that encode the K-channel proteins) through the targeting protein yotiao (another PKA anchoring protein), i.e., the PKA, its subunit PPI and the protein yotiao are components of the hKCNQ1 complex [12].…”